Environmental health secrets I written by Luanne K. Williams, Ricky Langley ... on
the toxicity of several PCB mixtures that have been commerciaUy available.
LUANNE KEMP WILLIAMS, PharmD Toxicologist North Carolina Department of Health and Human Services Division of Public Health Occupational and Environmental Epidemiology Branch Raleigh, North Carolina
RICKY L. LANGLEY, MD, MPH Medical North
Epidemiologist Carolina
Division
of
Occupational Raleigh,
Department
Public and
North
of
Health
and
Human
Services
Health Environmental
Epidemiology
Branch
Carolina
HANLEY &..BELFUS,INC. / Philadelphia
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Publisher:
HANLEY & BFLFUS, INC. Medical Publishers 210 South13d1Street Philadelphia,PA 19107 (215) 546-1293;800-962-1892 FAX (215)190-9330 Web site:http://www.hanleyandbelfus.com
Note to the reader: Although the infonnation in d1is book bas been carefully reviewed for cor~ of dosageand indications, neither the authors nor the editor nor the publisher can accept any legal responsibility for any errors or omissions that may be ~. Neither the publisher nor the editor makesany W8IT8Dty,expressedor implied, with respectto the material contained herein. Before pr'CSCribingany drug, the reader must review the manufacturer's cunent product information (packageinserts) for acceptedindications, absolute dosagerecommendations, and other infonnation pertinent to the safe and effective use of the product described.
Library of CongressCataloging-m-PubUcationData Williams, LuanneK. EnvironmentalhealthsecretsI written by LuanneK. Williams, Ricky Langley p. ; cm.-(I'he SecretsSeriese) Includesindex. ISBN I-S00S3-408-7(alk. paper) 1. Environmentalhealth-Examinations,questions,etc. 1 Langley, Ricky L., 19S7- n. Tide. m. Series. [DNI.M: 1. EnvironmentalHealth- ExaminationQuestions. WA 18.2 L283e 2(XX)] RAS6fJ.23 .1..362001
61S.9'0076-dc21
00-039652
ENVIRONMENTAL HBALm SECRETS
ISBN 1-5&>5.3-408-7
C2OO1 by Hanley & Belfus, Inc. All rights reserved. No part of d1is book may be reproduced, reused,republished, or transmitted in any foml, or stored in a data baseor retrieval system, without written pennission of the publisher.
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20. PERSISTENT~VIRONMENT AL CONTAMINANTS ::ait'in McArleton, B.S.,AndrewMaier, Ph.D., CIH, and Kenneth A. Poirier,Ph.D
HALOGENATED DIOXINS/fURANS
l. What are halogenated dioxinsandlorans? Dioxins and furans are related compoundscharacterizedby a siniilar backbonethat varies in ~ number and position of halogen atom substitutions, as shown in d1efigtue below. Although ~ are many fonDSof these compounds, the best known is 2,3,7,8-tetrachlorodibenzo-P-9ioxin CDD). TCDD is the most potent of this class of chemicals, and as a result d1ebiological actives of the other dioxins and furans are often described relative to that of TCDD. Only a small bset of the total dioxins and fuI3DS,however, are thought to induce health effects through the me mech!imsm of TCDD.
. Bow do these compounds get into the environment? Halogenated dioxins and furans are not thought to be naturally occurring. rather they are med asby-products of various industrial and combustion processes.Potential sourcesof release :heenvironment include chlorination processessuch as paper bleaching. manufactureof chloried organic chemicals. including some pesticides;and combustion of fossil fuels and municipal
I hazardous waste.Chlorinateddioxinsandfuranscanalsobepresentin cigarettesmoke..
Once thesecompounds are releasedinto the environment they are resistant to being degraded, I thus they tend to be persistent They are generally hydrophobic and for this reason they can .accummulatein the fatty tissues of animals that have ingested contaminated vegetation. soil. water. The diet, primarily in meat and dairy products. is thought to be the major pathway for Qnic low-level exposure in humans. 121
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3. Whatare: the primary
neaJ"theffects from exposure to dioxiDS and furans? TCDD is noted for the wide array of physiological systemsaffected. A hallmark symptom of
high TCDD exposurein humansis chloracne,a severeskin dL~~~ characterized by acnelikelesions. Chloracne bas beenassociatedwidl body burdens ofTCDD ranging from 18 to 2357 ng/kg body weight Erythematous or red skin rashes,discoloration, and excessivebody hair have also ~ reported to occur in people following exposure to high concentrations of TCDD. Mild and reversible altezabonsin the ability of the liver to metabolize hemoglobin, lipids, sugar. and IXOtein have been reported to occur in people following exposure to high concentrations of TCDD. Other effects have been less oonsistendyreported in people. It is not clear whether TCDD can induce adversereproductive or developmental effects in humans and die carcinogenicity data for TCDD have provided mixed results, with varying interpretations. The International Agency roc Researchon Cancer concluded that TCDD can cause cancer in humans and the U.S. Environ~tal Protection Agency (EPA) clu-~ifies TCDD as a possible human carcinogen. TCDD ~g bas been shown to iOOuceadvezseeffects in many target organSin Animal toxicity studies,.including a wasting syndrome,thymic atrophy and other immunological effects, and effects on reproduction and devel~ It should be noted that there is considerablevariability in speciessensitivity to the effects of TCDD, therefore for many end.points the applicability to exposedhumans remains unclear. . POLYCHLORINATED BIPHENYlS
4. What are polychlorinated biphenyk? The polychlorinatedbiphenyls(PCBs)are a group of 209 different compounds,referred to as congeners,characterizedby a similar chemicalbackbonethat varies in the numberand position of chlorine atoms(seefigure, question1). In most cases,PCBs are describedbased on the toxicity of severalPCB mixturesthat have beencommerciaUyavailable.Thesemixtures,called arochlors,are uniquemix.turesidentified by a numberindicating the numberof carbonatomsper moleculeandpercentageof chlorine in the mixture. For example,the U.S. EPA bas reviewed.the toxicity data for the developmentof human health risk values for arochlors1016,1248,and 1254. S. Bow do these compounds get into the environment? PCBs are not known to be naturally occurring. They once were manufacturedextensively fCK use as electrical insulators in tlansformers and capacitors. Although no longer used in theseproducts, PCBs can be releasedinto the eoviro~t by leaking from old electrical equipment dI8t still contains PCBs. These compoundscan also be generatedduring the combustion of municipal and industrial waste. Due to their hydrophobic Dabue,PCBs are Iesistaot to degradationin the environment, where they associatewith organic matter in seiI.JmenLSimilarly to dioxins and furans, PCBs bioaccuml~la'~in the adiposetissuesof anirnA1~that have ingested conbminat~ vegetation, soil, or water and in the diet, priuiarily in meat and dairy products. This Is thought to be the major pathway for chronic low-level exposure in humans. 6. What are the primary health effects of exposure to PCBs? Acute exposuresto PCBs have been associatedwith a variety of symptoms in exposedpe0ple. These include skin initation, ~ and rashes,neurological effects S1M:h as general weakness and numbness.respiratory initation following exposure by the inhalation route. altered immune function, and liver damage.Toxicity snldies in animal.. have shown a similar array of effects following acute exposures. In chronic animal exposure studies,PCB treabnent administered orally resulted in effects on the liver. stomach.and thyroid gland and decreasedreproductive ability. The human evide;nceis inconclusive regarding the ability of PCBs to causecancer, but animal smdies have reported increasedtumor incidence in PCB-treated anima1~.B~ on these data. the U.S. EPA classifies
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; as probable human carcinogens and the International Agency for Researchon Cancer bas mined that PCBs may reasonably be anticipated to be human carcinogens.
MERCURY What is mercury? 2ch year, anywhere from 2700 to ~ tons of mercury is released into the environment natural sources, and another 2000 to 3000 tons is contributed by human activities. Three s of mercury exist, each having different physical and chemical properties, routes of expoand health effects. The first is metallic mercury, or ~ in its elemental form. It appears , and silver and is a liquid at room temperature.Mercury vapor is releasedfrom the metal in :tate.The second form is a group of inorganic mercury compounds, or mercury salts. These >rmedwhen meICurycombines with other elementssuch asoxygen, sulfur, or chlorine. Most as powders or crystals. The third forDl is organic mercury, which is created when mercury >ines.with carbon-based molecules. The most common organic mercury com~und is ylmercury.
How are peopleexposedto inorganic (metallic and the inorganic salts) mercury? Brokenthemlometers.shatteredfluorescenttubes.or damagedelectrical switchescanexpeopleto metallic mercurythroughinhalationof the vapors.Breathingmercuryvaporsis lcern in closedareas.because80% of inhaledmercuryvaporis absorbeddirectly into the dstream.Swallowing metallic mercury is not as much of a health concern.becausethe .achor intestinesabsorbless than 0.01% of the dose.DerDlalcontactwith the metal can e rashes. How a.-epeople ~ to methylmercury? Microorganisms in the water can convert metallic mercury into methylmercury. Methyhnerbioaccumulates, and can be present in significant concentrationsin the tissuesoforg anisms the tops of food chains-shark, swordfish, and large tuna being several ex8Dlples.Cooking not appreciably reduce the methylmercury concentration in food. Methylmercury causesfelethylmercury poisoning, and can be passedin breast milk. alildren and fetuses are the most itive to exposure.
What are the effectsof mercury exposure? Mercuryimpactsthe nervoussystem.Rememberthe Mad Hatterin Alice in Wonderland? d asa hatter!" is a sayingdescribingmilliners who haddevelopedmercurypoisoningfrom . exposureto mercuriousnitrate, onceusedin the manufactureof hats.A variety of symp; are possiblefor exposureto the variousforms of mercury,and dependon degreeof exIre.Short-termexposureto metallic mercuryvapor can irritate and damagethe tissuelinthemouth and lungs, causinga burning sensationand tightnessof breath.Paresd1esia, a bnessand tingling sensationaroundthe fingers,toes,and lips, is usually an early nervous ~mmanifestationof exposure.The next progressivesymptomis characterizedby a diffi, walking andtalking, followed by a constrictionof visual fields, andfinally tunnelvision loss of hearing.Peoplemay demonstratenervousness, irritability, shyness,an inability to :entrate,and memoryloss. Severeexposurescan leadto tremorsor jerks. Kidney damage occur,especiallyafter exposureto toxic concentrations.Comaor deathis the end to this :ression.
Howcanexposureto mercurybemeasured? Mercury levels in the body can be measuredin blood. urine. or hair samples.Breast milk can be tested for mercury concentrations. Urine samplescan indicate exposure to metallic mer. vapor and to inorganic forms of mercury. whereaswhole blood and scalp hair mercury conrations correlate to methylmercury exposure.
Persistent Environmental Contaminants
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12. Is there health risk from mercury in dental fillings? Metallic mercury is often presentin dental amalgam, which is used in fillings. Although u.s. government evaluations conclude there is no health threat posed to the general population from dental amalgam, there is currently an investigation on the health risks for sensitive populations and the possibility of subtle immune or behavioral effects. PESTIODES
13. What are pestiddes,and what categoriesof pesticidesem? The United StatesEnvironmentalProtectionAgency defines pesticideas any substance or mixture of substancesintended for preventing,destroying, repelling, or mitigating any pest. There are five broad categories.The first category is insecticides, containing the organochlorine,anticholinesterase,pyrethroid. and botanical insecticides.Herbicides, the secondcategory, encompassthe chlorophenoxycompoundsand bipyridyl derivatives. The third categoryis fungicides, groupinghexachlorobenzene, pentachlorophenol,phthalimides, and dithiocarbamates.Fumigants composethe fourth category and include phosphineand ethylenedibromide/dibromochloropropane. The final and fifth categoryis the rodenticldes, including the zinc phosphide,fluoroaceticacid andderivatives,a-naphthylthiourea(ANTU), and anticoagulants. 14. How long have pestidda been u1ed? Pesticide use has been recorded for millennia. Homer recounted the use of sulfur for fumigation in 1 B.C. and in 200 B.C. Cato wrote about using sulfur to destroy vine pests. By ~ A.D., the 01inese were using arsenic to control garden insects. However, widespread chemical pesticide use did not become widely establisheduntil the mid-19th century. These precursors to modem pesticides included primarily inorganic comJK>unds such ascopper and mercury salts, sulfur, arsenic,and cyanide. Someorganic compoundswere used and included tar di-~t~ and oatural plant extIacts such as dersis (a root extract), nicotine, and pyrethrum. 15. What are the relative benefits and concerns of pestidde use? Many people believe that the useof pesticideshasbrought about positive changesfor humans such as improved food quality. decreasedfood prices. improved animal welfare and human health, and increasedproductivity. However. overuseof pesticides, contamination of water supplies. and the appearanceof residual pesticides in foodstuffs have raised the level of concern of health scientists and the public to the acute and chronic effects from pesticides (carcinogenicity. mutagenicity. teratogenicity. immune systemeffects. and central nervous systemeffects). As we better understand die potential human and ecological healdt effects of the pesticides. govem~ntal regulatory agenciescan apply more prudent measuresto balance dle concern of pesticide use widt the perceived societal benefits.
16. How do peoplecomeintocontad with pestiddes? Pesticidesare in usein agriculture,homegardensand lawns, in homes,andin somepublic placessuchas parks or airplanes.The mostlikely population to be exposedto potentially unsafelevels is the occupationally exposed,such as farmworkers or workers in a pesticide manufacturingplant. Exposurecan occurby dermal,oral, or inhalation routes.In extremesituations,poisoningscan occur. Residuesof pesticideshave beenfound on food, such as produce. 17. Why are pesticides considered toxic, and what are the modes of action? Pesticideswere developed to be toxic to specific living things, be it vertebrates,invertebrates. or microorganisms. The chemical compounds that make up each pesticide have a certain effect on biological systems. ideally impacting only the target organism. Unfortunately. nontarget speciesfrequently are affected becausetheir physiological and/or biochemical systems are simi-
125
, those-1)fthe target species.Each of the different classesof pesticides has a different mode tion. For example, exposure to organochlorine and anticholinesteraseinsecticides, of which 'dane,dieldrin. and methoxychlor are members,can result in central nervous system effects. urces for pesticide poisoning guidance include the National Pesticide Telecommunications 'ork (NPTN) at 800-858-7378 (internet site: www.ace.OISt.edu/info/nptnfmdex.html)and the ician's Guide to Pesticide Poisoning, available online at www-aes.tamu.edu/doug/MED/ P.htm. DDT (P ,P' -DICHLORODIPHENYL
TRICHLOROETHANE)
:sDDT still a poDutant or coucem in the United States? )DT was recognized to have insecticide properties in the late 1930s and was used exteny in the United States until its ban in 1972. Since that time, levels of DDT in the environin many parts of the United States have decreased;however, DDT is still Used in other of the world and atmospheric deposition of DDT represents a source of current contamin. In addition. DDT undergoes a gradual breakdown in the environment to DDE. There:ontaminated sites can still have significant levels of both DDT and DDE arising from pesticide use. Because of its continued international use and environmental persistence, ;~ to DDT and DDE can result from consumption of contAminAt~ fish, crops grown in minated soil, or imported crops that were sprayedwith DDE. Lactational transfer is a path'or exposure of infants. ~t caused DOT to be banned? D 1962, Rachel Carson published "Silent Spring," warning the world about the widespread If more appropriately, misuse) of pesticides.Subsequently,DDT was shown to interfere widt aell-makiog capability (reproduction) of avian wildlife, causing a dramatic decreasein the anon of many birds, including the American bald eagle. As a result, DDT was banned for I the United States. Vhat health effects are ~ted with DDT and DDE? imiIarly to other persistent chlorinated pollutants, DDT has been associatedwith liver and logical effects. The evidence for carcinogencity is mixed in human epidemiology studies, !sedon positive results in anima) studies,the U.S. BPA bas classified DDE as a probable hu:arcinogen.A primary effect of concern is the potential adversereproductive effects ofDDT IDE. Although the human evidence for adverseeffects are not conclusive, a variety of adeffects have been reported in anima) toxicology studies. CONTROVERSY
U eatingsportfish leadto a significanthealthrisk? lany persistent environmental pollutants can bioaccumulate in wildlife that are exposed to ninated environments. Based on the recognition that human exposwes to pollutants can be .cantfrom eating fish, the U.S. EPA and many stateagenciesestablish fish consumption ad~. Advisories have been established for many bodies of water and are based on levels of ants such as mercury, PCBs, dioxins, chlordane, and DDT, among others. FISh consumplvisories are available though ~ U.S. EPA data basesor from statehealth or environmen~ncies. Ithough the potential for adverse effects of eating highly contAminAtedfish is clearly rec--d,the trade-off between risk from low levels of these pollutants and the health risk from toting fish with less healthy dietary alternatives is uncertain and an area of active research. It wod focuses on development of methods to assessthese comparative risks.
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BlBUOGRAPH¥-
1. Agency for Toxic Substancesand DiseaseRegistry: Toxicological profile f« cbI~ dibenzo-p-dioxiDS.U.S. ~ of Health and Human Services.WashiDgtoo.D.C., U.S. Govt. Printing Office, 1998. 2. Agency for Toxic Substancesand DiseaseRegistry: Toxicological POfile f« 4,4' -DOT, 4,4' -DOE, 4,4'ODD. U.S. Dept. ofHealtb and Human Services.Washington. D.C., U.s. Govt. Printing Office, 1994. 3. Agax;y f« Toxic SubstaJx:eS and Disease Registry: Toxico1ogica1.-ofile f« uacvry. U.S. ~ of Health and Human Services.Washington, D.c., U.S. Govt. Printing Office, 1999. 4. Agency for Toxic Substancesand DiseaseRegistry: Toxicological.-ofile for p>lycblcxiuatedbipbenyls. U.S. ~ ofHealtb BOOHuman Services.WashiDgtoo.D.C., U.S. Govt. Printing Office, 1.997. 5. AIbuck1e Tf., SeVei'L.E: Pesticide exposuresand fetal dead1:A Ieview of the epidemiologic literatme. Crit Rev Toxicol 28(3): 229-270, 1998. 6. Ecobicboo OJ: ToxM:effects ofpestic ides. In KJasseoCD (ed): CasaIett aOODoull's Toxicology: The Basic ScieDceofPoisioos. New York, McGraw-HiD, 1996. 7. Orloff KG, FagIiaDOJ, U1inch G et aL: Human exp)8UIe to e~'31 mercury in a cont.mioat~ ~dential building. Arch Environ Health 52(3): 169-1n, 1.997. 8. Toxicology Excellence for Risk Assessment:Comparative dietary risks: Balancing the risks and benefits of fish coosumptioo. 1999. Intemet site: bUp://www.tcra.cxg. 9. U.S. Environ_tal Protection Agency: National listing of fish aOOwildlife advisories,FJ»A-823-F-99005,1999. Internet site: http://www.epa.gov/ost/fish/. 10. U.S. Environmental Protection Agaw;y: Unified Air Toxics Website, 1999; ODE (p.p-dkhl
